
DHA-enriched phosphatidylcholine suppressed angiogenesis by activating PPARγ and modulating the VEGFR2/Ras/ERK pathway in human umbilical vein endothelial cells
Author(s) -
Yuanyuan Liu,
Yingying Tian,
Yinglu Guo,
Zhe Yan,
Changhu Xue,
Jingfeng Wang
Publication year - 2021
Publication title -
food science and biotechnology/food science and biotechnology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.595
H-Index - 38
eISSN - 2092-6456
pISSN - 1226-7708
DOI - 10.1007/s10068-021-00990-0
Subject(s) - angiogenesis , umbilical vein , mapk/erk pathway , chemistry , chorioallantoic membrane , neovascularization , cd36 , microbiology and biotechnology , peroxisome proliferator activated receptor , biochemistry , receptor , signal transduction , biology , cancer research , in vitro
Docosahexaenoic acid-enriched phosphatidylcholine (DHA-PC) is a new generation of omega-3 lipids, which contains an ester bond linking DHA at the sn-2 position of phospholipid. DHA-PC has become the interest recently as its better bioavailability and anti-oxidation capacity. In this study, the anti-angiogenic effect of DHA-PC was evaluated. The capacities of proliferation, migration, tube formation of human umbilical vein endothelial cells were significantly declined after DHA-PC treatment. Furthermore, DHA-PC inhibited the neovascularization of the chick chorioallantoic membrane in vivo. Mechanism results indicated that DHA-PC enhances the expression of peroxisome proliferator-activated receptor γ (PPARγ) at transcriptional and translational level, subsequently down-regulates the VEGFR2 expression and VEGFR2-mediated downstream Ras/ERK pathway, resulting in significant reduction in proliferation and differentiation. Additionally, PPARγ-specific antagonist GW9662 partly reversed the inhibition effects of DHA-PC on tube formation and neovascularization, suggesting that DHA-PC exerts anti-angiogenesis effect through activating PPARγ. These findings indicated that DHA-PC has a great prospect of anti-tumor angiogenesis therapy.